ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2017
The Alu neurodegeneration hypothesis: A primate-specific mechanism for neuronal transcription noise, mitochondrial dysfunction, and manifestation of neurodegenerative disease.
Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
35 citing papers in PubMed, 69 citations in OpenAlex.
- Alu-mediated SPAST deletion impairs golgi zinc transport and reveals a druggable vulnerability.Signal transduction and targeted therapy · 2026Article
- Long-read sequencing maps transposable element variation and its regulatory and epigenetic effects in the human brain.bioRxiv : the preprint server for biology · 2026Article
- Alzheimer's disease: genetic background in the era of next-generation sequencing technologies.Brain communications · 2026Review
- Single-Cell Transcriptome Patterns of Transposable Elements in Alzheimer's Disease.Molecular neurobiology · 2025Article
- Notable challenges posed by long-read sequencing for the study of transcriptional diversity and genome annotation.Genome research · 2025Review
- Transposons disrupt genomic stability and trigger cancers.Frontiers in cellular and infection microbiology · 2025Review
- From Diabetes to Dementia: Identifying Key Genes in the Progression of Cognitive Impairment.Brain sciences · 2024Article
- Review
- Correlation of Myeloid-Derived Suppressor Cell Expansion with Upregulated Transposable Elements in Severe COVID-19 Unveiled in Single-Cell RNA Sequencing Reanalysis.Biomedicines · 2024Article
- Pharmacogenomics of Dementia: Personalizing the Treatment of Cognitive and Neuropsychiatric Symptoms.Genes · 2023Review
- Repetitive DNA sequence detection and its role in the human genome.Communications biology · 2023Review
- Exonized Alu repeats in the 3'UTR of a CYP20A1_Alu-LT transcript act as a miRNA sponge.BMC research notes · 2023Article
- The Role of Transposable Elements of the Human Genome in Neuronal Function and Pathology.International journal of molecular sciences · 2022Review
- AnNAR genomics and bioinformatics · 2022Article
- Genome-wide perturbations of Alu expression and Alu-associated post-transcriptional regulations distinguish oligodendroglioma from other gliomas.Communications biology · 2022Article
- The role of structural variations in Alzheimer's disease and other neurodegenerative diseases.Frontiers in aging neuroscience · 2022Review
- Alu RNA and their roles in human disease states.RNA biology · 2021Article
- Increased Alu RNA processing in Alzheimer brains is linked to gene expression changes.EMBO reports · 2021Article
- Retrotransposons as Drivers of Mammalian Brain Evolution.Life (Basel, Switzerland) · 2021Review
- The TOMM40 '523' polymorphism in disease risk and age of symptom onset in two independent cohorts of Parkinson's disease.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
It is hypothesized that retrotransposons have played a fundamental role in primate evolution and that enhanced neurologic retrotransposon activity in humans may underlie the origin of higher cognitive function. As a potential consequence of this enhanced activity, it is likely that neurons are susceptible to deleterious retrotransposon pathways that can disrupt mitochondrial function. An example is observed in the TOMM40 gene, encoding a β-barrel protein critical for mitochondrial preprotein transport. Primate-specific Alu retrotransposons have repeatedly inserted into TOMM40 introns, and at least one variant associated with late-onset Alzheimer's disease originated from an Alu insertion event. We provide evidence of enriched Alu content in mitochondrial genes and postulate that Alus can disrupt mitochondrial populations in neurons, thereby setting the stage for progressive neurologic dysfunction. This Alu neurodegeneration hypothesis is compatible with decades of research and offers a plausible mechanism for the disruption of neuronal mitochondrial homeostasis, ultimately cascading into neurodegenerative disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.